Glossary of 525 patho exam 2
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- How do we know that neurons are metabolically active cells?
- large nucleus
a lot of mitochondria
produce alot of ATP
require an abundant supply of O2
(lack of O2 for more than 4 minutes = cell death)
- What is the carcinogenic potential for neurons?
- Low - because they are postmitotic
- Characteristics of spinal motor neurons.
- Extend out away from spinal cord, cell body in ventral horn, super long.
- Characteristics of spinal sensory neurons.
- Dorsal root ganglion receives input.
- Characteristics of cranial nerves.
- Motor neurons serving the head and neck, interface with the medulla or brain stem.
- Where are upper motor neurons found?
- cerebral cortex
- What is a ganglia?
- collection of cell bodies of upper motor neurons in the cerebral cortex.
- bring input into cell body
- take information away from cell body
- connection between 2 neurons
- How is communication mediated between neurons at a synapse?
- chemically - with a neurotransmitter
- substance that is released by a presynaptic neuron (in response to an AP in that neuron) that diffuses across the gap to the postsynaptic neuron, binds to a receptor and elicits a response in the postsynaptic neuron.
- Common examples of neurotransmitters
- acetylcholine, norepinephrine and dopamine are most common examples of neurotransmitters
- The connection between neurons may be ---------- or --------- depending on the events that occur in the postsynaptic cell in response to the neurotransmitter
- The connection between neurons may be excitatory or inhibitory depending on the events that occur in the postsynaptic cell in response to the neurotransmitter
- What is the aim of modern neuropharmacology?
- Modern neuropharmacology is aimed at maintaining or restoring normal neurotransmitter balance within neurons of the brain.
- The support cells of the CNS:
- Glia (neuroglia):
3.Microglia – not discussed
- All of the support cells in the CNS are...
- facultatuve mitotic cells
- Large star shaped cells, cytoplasmic processes link neurons and blood vessels
1.function in metabolism of neurotransmitters
2.help to form the blood brain barrier (BBB)
3.function to maintain extracellular fluid balance
*network of support for neurons because no lymphatic system in brain
- Cytoplasmic processes of myelinated nerve fibers. myelin- insulation – make transmitting AP faster
In peripheral nervous system, Schwann cells are equivalent
Myelin allows for very rapid conduction of AP’s
-regulate extracellular fluid like astrocytes
-most common glial cell (essentially a lipid layer coating the axon)
- gray – unmyelinated, neural cell bodies
white – myelinated, cellular processes (no cell bodies)
Myelin serves to insulate the neuron and allows for increased speed of the AP propagation
*Some disease states affect the myelin sheath - MS
- What cells line the ventricles and central canal of the spinal cord and have cilia to promote flow of CSF?
- Ependymal Cells
- what makes up the Central Nervous System?
- brain and spinal cord
- What makes up the Peripheral Nervous System?
- Peripheral sympathetic and parasympathetic nerves and the autonomic ganglia.
- What are the 3 distinct brain regions?
- Hindbrain (most primitive, 1st to develop) - medulla, pons, cerebellum
Forebrain - cerebrum, thalamus, basal ganglia, hypothalamus
- What functions is the frontal lobe associated with?
- motor, problem, solving, spontaneity, memory, language, initiation, judgment, impulse control, social and sexual behavior
- Functional regions of the parietal lobe.
- 1.sensation and perception
2.integrating sensory input, primarily with the visual system
- Function of occipital lobe.
- vision and the interpretation of vision
- Function of temporal love.
- auditory sensation, language, and perception
- Function of basal ganglia.
- integration centers for sensory information ascending to the cortex and motor information descending to lower levels;
monitors what SHOULD BE occuring with WHAT IS occuring;
Coordinating muscle movement (fine adjustments)
- Function of amygdala.
- center for emotions (fear, confusion, distrb. awareness, amnesia, rage)
- Function of hippocampus.
- short term memory, spatial orienting/processing info as it enters the brain;
largest neurons-prone to ischemic attack (result: s-t memory loss)
- Function of thalamus.
- integrating sensory stimuli;
acquisiton of knowledge and awareness
- Function of hypothalamus.
- integration of temp., HR, BP, thirst, appetite;
releases neurosecretory substances which activate pituitary (via neurons) to release hormones
- Function of hindbrain.
- 1st part to evolve;
pons, medulla oblongata, cerebellum
- Function of pons, medulla oblongata.
- -most primitive
-visual/auditory reflex ctrs.
-rate/force of contraction
-vasomotor center-BV tone
-respiratory ctrs. - rate
-origin of most cranial nerves
- Function of the cerebellum.
- major integrator of motor function
-damage to the cerebellum affects coordination of limb and eye movement
-compares what should be occurring with what is actually occurring - sends error messages to other areas
-determine our position in time and space
-damage results in ataxia, dysmetria, diffulting moving quickly, delayed initiation/termination
- postural instability
- disturbance of the trajectory or placement of a body part during movement
- Function of the midbrain (mesencephalon).
- all ascending and descending information to or from the cerebral cortex must pass through
- Function of the peripheral nervous system.
- nerves from CNS and the autonomic nervous system, including cranial nerves
- Function of the spinal cord.
- outer white matter and inner gray (opposite of brain tissue)
gray - neuron cell bodies
white - myelinated fibers and unmyelinated from ascending sensory or descending motor neurons
-motor root - going out
-sensory root - coming in
dorsal root ganglion - cell bodies for all sensory nerves
- Function of Meninges.
- protective covering of brain and spinal cord.
-brain injury will result in bleeding in at least one of the layers
- Function of Cerbrospinal Fluid (CSF).
- Produced in choroid plexus (a series of specialized capillaries, it flows throughout the ventricular system and exits through lateral openings or a medial opening into the subarachnoid space (bathes brain, cushions brain).
-Can also enter the central canal of the spinal cord.
-fast turnover (3x a day)
-distinct composition and pressure - alterations in ions, cells, pressure indicate disease
- An increase in CSF pressure is caused by ...
- -increased polymorphonuclear leukocytes - bacterial infection (and acute inflammation)
-increased lymphocytes - viral infection (meningitis)
-decreased glucose concentration - bacterial infection (meningitis) – bac. use glucose for food
- Function of Blood Brain Barrier
- -capillary endothelial cells and glial (astrocyte) cellular processes make a thick basement membrane
-glucose, alcohol, amino acids, oxygen and carbon dioxide readily penetrate
-diffusion of lipids limited by size - one reason the brain can not metabolize fat to produce ATP – only glucose!
-only certain antibiotics gain access to brain: erythromycin and sulfadiazine
-insulin cannot cross
- How is blood supplied to the brain?
- internal carotid --> circle of Willis on base of brain (circles the stalk of pituitary)
vertebral arteries, R & L vertebrals merge to form basilar; serve the pons, medulla, cerebellum
- 3 major branches from the circle of Willis:
- 1.Anterior cerebral - supplies structures on the front of the brain
2.Posterior cerebral - supplies the back of the brain
3.Middle cerebral - supplies almost all of the lateral aspects of the brain – the largest portion
- Inability to comprehend and integrate receptive language or use language or both.
-∑ associated with lesions to the dominant cerebral hemisphere
-extent of the lesion(s) determine(s) the extent of damage
- Wernicke’s Aphasia
- damage to area where understanding and interpretation of word symbols occurs (in the dominant hemisphere);
lesions result in impairment in comprehension of speech
-patient is unaware of a problem
-affected persons have fluent, spontaneous speech with normal rhythm and articulation - word salad
-comprehension, repetition and naming are impaired
- Broca’s Aphasia
- Lesion located in frontal lobe just in front of motor area
-individual may not be able to utter a word or have limited speech
-fully comprehends spoken word
-fully aware - FRUSTRATION
- Global Aphasia
- -large lesions to both Broca and Wernicke’s area in dominant hemisphere
-DUE TO MAJOR BLOCKAGE OF MIDDLE CEREBRAL ARTERY
-all aspects of speech involved
-patients usually have hemiplegia and are unable to comprehend or speak
- Which hemisphere is dominant in most people?
- >90% of right handed people are left hemisphere dominant
- loss of function and this includes both spastic and flaccid paralysis;
usually defined in terms of injury to upper motor neurons and lower motor neurons
-Upper at higher levels of the brain and spinal cord
-Lower at the level of the spinal cord OR peripheral nerves
- 2 types of paralysis
- 1.Spastic paralysis – muscles are hard, rigid and difficult to move a joint; can exhibit hyperactive reflex activity
2. Flaccid paralysis – muscles flaccid with lack of reflex activity
- Characteristics of Upper Motor Neuron Injury
- Spastic paralysis, hyperreflexia, Babinski sign, muscle atrophy (develops over a few weeks)
- Characteristics of LMN injury.
- Flaccid paralysis - loss of muscle tone
loss of peripheral reflexes occurs
-significant and prompt muscle atrophy
- What is the most common CNS malformation?
- Neural tube defects - failure of the neural tube to fuse.
- When does closure of the neural tube start and finish?
- start: 22nd day, finishes: 28th day of gestation
- This is a catastrophic defect resulting in failure of the brain to develop.
- Anencephaly - cerebrum does not develop, most common neural tube defect (1/500 preg.) May be carried to term but infant dies soon after. Higher in women over 40 (Ireland sees it in 1/200.) preg.)
- A group of neural tube defects in which the area affected is in the lower back.
- Spina Bifida - 4 kinds
Occulta (mildest; hair)
Rachischisis (most severe)
- What is Spina Bifida Occulta?
- This defect is a lack of development of vertebral arches. Skin usually covers the defect- hair usually seen over the defect. Neural elements are in the normal location.
- What is Meningocele?
- Protrusion of meninges (ballooning) through a defect in the spinal column. Neural elements in normal location.
- What is Myelomeningocele?
- Protrusion of meninges (ballooning) through a defect in the spinal column with protrusion of cord elements.
- What is Rachischisis?
- Most severe form neural tube fails to close and open to the elements, brain is open to infection.
- What nutrient reduces incidence of neural tube defects?
- folic acid - essential for formation of nucelotide base thymine.
- What should women of reproductive age who are sexually active should take a supplement of folic acid?
- Because whether they intend to become pregnant, if they do, defects would occur prior to time woman knows she is pregnant.
- What are the types of traumatic head injury?
- What is a concussion?
- Blunt head trauma characterized by loss of consciousness; no significant macroscopic or microscopic changes to the brain.
- What is a contusion?
- Disruption of cerebral and/or meningeal blood vessels by severe blunt trauma; associated with considerable mortality.
- What is a laceration?
- Open trauma to the brain tissue; highly fatal.
- What is cerebral edema?
- Fluid accumulation within the brain;
two types: cytotoxic and vasogenic - closely related.
- What is cytotoxic edema?
- Cellular dysfunction or injury due to loss of cellular ability to regulate water.
Anything that causes loss of ATP to power the pumps will result in cytotoxic edema. If Na/K pump fails then Na accumulates --> water follows.
- What can cause the loss of ATP to run Na/K pumps?
- What is vasogenic edema?
- Edema characterized by increased vascular permeability from damage to or dysfunction of cerebral vessels.
-composition of the fluid is similar to plasma – plasma proteins and it accumulates in the interstitial space.
-this protein draws fluid by osmotic forces
-lack of blood flow results in cytotoxic edema
- Vasogenic edema results in...
- cytoxic edema.
- What are the clinical signs of cerebral edema?
- increased intracranial pressure --> decreased cerebral blood flow --> decrease in cerebral function --> hernaitions of the brain (through foramen magnum)
-brain appears heavy; wet
-sulci are obliterated, ventricles flattened, subarachnoid space lost.
- This is frequently seen in shaken baby syndrome or following major trauma to the brain.
- Cerebral edema
- This is a lay term for the slow or sudden onset of a series of neurological symptoms; a disease of old age and related to atherosclerosis of cerebral arteries.
- What causes stroke?
- 1.Occlusion of cerebral vessels - from atherosclerotic narrowing of an artery, thrombus formation or lodgement of an embolism, or by
2.hemorrhage - from intracerebral, subarachnoid or AVM (arteriovenous malformations) bleeding.
- What are factors that favor the development of stroke?
- hypertension, diabetes and thromboembolism
- What is the result of stroke?
- ischemia and necrosis to the brain
- What is a TIA?
- Transient Ischemic Attack - lasts for a few minutes to a few hours and the neurological deficits resolve.
-first sign of atherosclerotic narrowing or cerebral vasoconstriction
- What is occlusive cerebrovascular disease?
- Includes atherosclerosis, cerebral thrombosis (usually of an atherosclerotic plaque) and cerebral embolism
-these have a final common pathway, even though pathogenesis of each is different.
- What is cerebral atherosclerosis?
- cerebral arteries undergo the process of atherosclerosis -->
formation of an atheroma that projects into the vessel lumen --> inhibits blood flow --> ischemia
-primary cause of TIAs
-if lesion ruptures --> thrombus forms --> aggravates vessel narrowing
- What is the leading cause of CVAs?
- Cerebral Thrombosis
- Where do cerebral thromboses usually cause an occlusion?
- curves and bifurcations of vessels - why? turbulence --> endothelial injury
- How quickly can cerebral thrombosis occur?
- gradual: thrombus forms on existing plaque over time causing occlusion
rapid: ischemic infarction from an embolus dislodged from an atherosclerotic plaque that moves to the brain.
- What is the usual cause of death with cerebral thrombosis?
- cerebral edema (3-5 days later) from both cytotoxic and vasogenic mechanisms
- The clinical presentation of cerebral thrombosis.
- gradual or more rapid occlusion of middle cerebral artery (#1 cause) results in contralateral hemiplegia,
sensory loss, bilateral symmetrical loss of vision in half of the visual field, headache, vertigo, confusion, aphasia, other focal neurological signs
-global aphasia can occur if dominant hemisphere affected
-GRADUAL ONSET OF SYMPTOMS
- Characteristics of cerebral embolism.
- -source from heart due to atrial fibrillation, bacterial endocarditis, valvular disease
-also from dislodged thrombus on atherosclerotic lesion
-can cause massive infarction
-SUDDEN ONSET OF SYMPTOMS
- What is hemorrhagic cerebrovascular disease?
- intracranial bleeding.
ex: intracerebral hemorrhage, aneurysms
- What is an intracranial hemorrhage?
- rupture of blood vessel due to congenital abnormality (aneurysm); rupture caused be traume or through other mechanism like HTN.
-4 groups based on location
epidural, subdural, subarachnoid, intracerebral
- What is an epidural hematoma?
- Hematoma located between the skull and dura usually due to tear in a meningial ARTERY.
-causes pressure on brain, coma, and death
-DELAY ON ONSET OF SYMPTOMS
Tx - drill hole in skull to drain blood
- What is a subdural hematoma?
- Hematoma located between the dura and the arachnoid layer, usually due to rupture of thin walled bridging VEINS that traverse this area.
-MUCH SLOWER DEVELOPMENT THAN ARTERIAL BLEED (epidural h.)
- What is a subarachnoid hemorrhage?
- Ruptured cerebral vessels due to: arteriovenous malformations or rupture of berry aneurysms caused by trauma to cerebral vessels on the surface of the brain.
-BLOOD IN CSF (arterial bleed in subarachnoid space)
- What is an intracerebral hemorrhage?
- bleeding within the brain; results from rupture of small vessels damaged by HTN. Common site is basal ganglia.
Presents like cerebral embolism but more dramatic and severe headache.
- Berry Aneurysm - subtype of hemorrhage in the subarachnoid space. A defect of weakness of cerebral arteries --> outpouching. Originate in circle of Willis --> can be silent then rupture with HTN.
S&S: blood in CSF, very different treatment if hemorrhagic (vs. occlusive)
- Neoplasms of the CNS
- These are relatively rare, and can occur at any age but more prominient in youth and elderly.
50% tumors are primary
50% are metastatic
- Why are malignant neoplasms of the CNS hard to treat?
- Difficult to differentiate normal brain from the highly infiltrative malignant tumor.
- Why do primary malignant tumors not metastatize?
- Because of the BBB, no lymphatics in the brain.
- Clinical manifestations of intracranial tumors:
- highly variable
headache, vomiting, papilledema (eyes - fundus bulging)
paralysis, seizures, memory loss, visual field defects, cranial nerve dysfunction, mental status, speech disorders, tongue dev. to one side
- Classification of CNS tumors
- tumors of glial cells (75%)
tumors of the meninges (15%)
- a type of astrocytic glioma; occure as
1.solid cerebral tumors in adults
2.cycstic cerebellar tumors in children
-slow growing, well-differentiated astrocytes
- Glioblastoma multiforme
- -Most common CNS malignancy
-more malignant than astrocytomas
-peak incidence at age 65
-irregular shape, pooly demarcated from normal brain parenchyma
-highly infiltrative and vascular tumor, very rapid growth, no resemblance to parent cell
-in cerebral hemispheres - usually frontal lobe, in middle-age adults
-lesions well circumscribed, cystic, calcified (dystrophic)
- tumors derived from ependymal cells
-malignant and benign
-ventricular ependymomas in children
-spinal ependymomas in young adults
S&S: muslce weakness, disuse atrophy, sensory loss
- Prognosis of gliomas
- gliobastoma multiforme - fatal
astrocytomas - 5 yrs (poor)
cerebral oligodendrogliomas & ependymomas - better, but needs early detection
- tumor of the meninges
-benign lesion - in women after 70
-S&S: seizures, headache, visual impariment, hemiparesis, aphasia, compression of brain
-can be surgically removed; excellent prognosis
- metastatic tumors
- spread from other sites - usually lung (45%) breast (20%)
- Agents of CNS infection
- bacteria, viral, protozoal, fungal
-acquired by direct extension via the blood, through the blood and via nerves
- Common bacterial causes of CNS infection:
- N. meningitidis (meningococcus) and S. pneumoniae, E. coli, H. influenzae, T. pallidum
- Common viral causes of CNS infection:
- measles, rubella or adenovirus, CMV, herpes virus, rabies virus, arbovirus (mosquito vector) resulting in various forms of encephalitides (St. Louis, California, Venezuelan, etc), HIV, west Nile Fever, Dengue Fever
- Mad Cow Disease
- at least 2 forms of prions have been identified
-spread in animals by feed infection with neural tissues of infected animals
-brain has spongy appearance
- infection of brain parenchyma; usually viral invasion of neural and glial cells
- inflammation of the meninges
- Viral Meningitis
- T-lymphocytes fight virus --> exudate rich in T cells in subarachnoid space and CSF
-NO change in glucose
- Bacterial Meningitis
- exudation of neutrophils into subarachnoid space and CSF
-LESS glucose (it is used by the bacteria)
-S&S: stiff neck (nerves irritated by the infection)
- Multiple Sclerosis
- demyelinative disease affects 250,000 Americans, usually women 20-45 of Northern European origin who live in temperate climate zones above the 40th parallel
-clustering (NW Ohio)
- Clinical Features of MS
- recurrent episodes of neurologic symptoms
-sensory (touch) and motor (weakness) abnormalities
-Dx 2 separate sets of CNS symptoms
*Upper motor neuron injury
- Pathology of MS
- lesions infiltrated with T cells and macrophages in PLAQUES, oligodendroglial cells are gone (no insulation)
-Tx with corticosteroids, immunosupressives to SLOW
- Neurodegenerative diseases
- neuron cells themselves die (different from MS)
- form of dementia - atrophy of the corticol parts of the frontal and temporal lobes
-50-60% of people over 85
-loss of brain neurons that use acetylcholine as a transmitter affected
-LONG course, die from some other disease
-Dx only with exam of cortex so Dx is with the presence of progressive dementia
- -subcortical (other than the cortex) neurodegenerative disorder
-movement disorders; decreased numbers of dopaminergic neurons in the substantia nigra – a part of the midbrain
-tremor, rigidity, bradykinesia postural instability
- utosomal (chromosome 4) dominant neurodegenerative disease characterized clinically by choreiform movements and progressive dementia. (Chance 50/50 of getting)
-atrophy of the cortex and subcortical basal nuclei (caudate and putamen)
-appears in the 40s and rapidly deteriorates
- - irregular, spasmodic involuntary movements of the limbs or facial muscles often accompanied by hypotonia (decreased muscle tone)
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